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ESA 3 > Infection 7 > Flashcards

Infection 7 Flashcards

1
Q

Give examples of surfaces found on patients

A

Skin (And accessory nairs, hair)

Mucosa:

GI

Resp

Conjuctiva

Genitourinary

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2
Q

Give examples of viruses found living on the skin under physiological conditions

A

Papilloma

Herpes simplex

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3
Q

Give examples of normal skin bacterial commensals

A

Gram positive:

Staph aureus

Coagulase negative staphylococci

Gram negative:

Enterobacteriaceae

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4
Q

Give examples of normal skin fungi and parasites

A

Fungi:

Yeast

Dermatophytes

Parasites:

Mites

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5
Q

How can commensals become harmful?

A

Immunocompromise

Spread to another site

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6
Q

By what methods can pathogenic microbes cause infection/enter the body?

A

Invasion:

Strep pyogenes pharyngitis

Migration:

E. coli UTI

Innoculation:

Coagulase (-) staphylococcus prosthetic joint infection

Haematogenous:

viridans strep endocarditis

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7
Q

Give examples of internal and external surface infections

A

External:

Cellulitis

Pharyngitis

Conjunctivitis

Gastroenteritis

UTI

Pneumonia

Internal:

Envovascular (Endocarditis, vasculitis)

Septic arthritis

Osteomyelitis

Empyema

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8
Q

Give examples of prosthetic surface infections

A

Urethral catherter (most common HAI)

Intravascular lines

Peritoneal dialysis catheters

Prosthetic joints

Cardiac valves

Pacing wires (Endocarditis)

Endovascular grafts

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9
Q

What are the common causative organisms of endocarditis?

A

Native valve or >1yr post operation for prosthetic replacement:

viridans Strep

Enterococci faecalis

Staph aureus

Candida albicans

Prosthetic valve <1yr post op:

Coagulase (-) staph

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10
Q

What are the common causative organisms for infection from prosthetic joints?

A

Coagulase (-) staph

Staph aureus

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11
Q

What are the common causative organisms for infections from cardiac pacing wires?

A

Coagulase (-) staph

Staph aureus

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12
Q

What are the processes involved in pathogensis of infection on surfaces?

A

Adherence to host cells or prosthetic surface

Biofilm formation

Invasion and multiplication

Virulence factors actions and host response

Host response may be pyogenic (Neutrophils/Pus) or granulomatous

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13
Q

What is a biofilm?

What are their functions?

A

An aggregation of microbes on a surface surounded and encased in a slime matrix

Functions:

Create a favourale environment for growth, replication and exhange of chemical messengers allowing regulation of the colony as a whole

Protection from harmful substances and cells (E.g. Antibiotics and WBCs)

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14
Q

How is a biofilm formed?

A

Motile bacteria attach to a surface (aided by Pili/Fimbriae in some cases)

Attached bacteria multiply and produce a slimy matrix

Nutrients diffusie into the matrix and chemical gradients are produced that create microenvironments ideal for the bacteria

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15
Q

What is quorum sensing?

A

The co-ordination of bacteria in a colony to produce behaviours such as biofilm production, incresing virulence and antimicrobial resistance

This is a acheived through local signalling molecules (Autoinducers) and cell surface receptors allowing bacteria to sense the density of the local population and co-ordinate behaviours to adapt to that via changing gene expression

Changes in gene expression made across an entire colony of bacteria allow co-operative behaviours such as those mentioned above

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16
Q

How is diagnosis of surface infections approached?

A

Aim to identify organism and antimicrobial susceptibilities

This can be achieved through:

Blood cultures

Tissue biopsy

Sonification of prosthetics to disrupt bacterial biofilm and allow accurate diagnoses

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17
Q

What are the challenges of bacterial surface infection diagnoses?

A

Adherence of organisms to tissue/prosthetic, possibly in a biofilm

Low metabolic state in biofilms

Small colony variants of species in a biofilm amke antibiotic susceptibility harder to assess

18
Q

Outline a general management plan for a patient with a surface infection

A

Sterilise tissue and reduce bioburden

Antibacterials

Removal of prosthetic

Surgery (resection of infection/Infected material)

19
Q

What challenges are presented by surface infections to management of that infection?

A

Poor antibiotic penetration into the biofilm

Low metabolic activity in biofilm

Dangers/difficulties of surgery

20
Q

What are the principles of prevention for surface infections?

A

Natural surface/tissue:

Maintain surface integrity

Prevent colonisation

Remove colonising bacteria

Prosthetic surfaces:

Prevent contaimination

Inhibit surface colonisation

Remove colonising bacteria

21
Q

Define ‘Hypersensitivity’

A

An antigen specific immune response that is innappropriate or excessive and results in harm to the host

22
Q

What are the 2 phases of hypersensitivity development?

A

Sensitisation:

First encounter with antigen

Effector:

Clinical pathology results from second exposure to same antigen

23
Q

List the types of hypersensitivity reaction and the time frame within which it occurs post exposure

A

Type 1 - Immediate (<30mins)

Type 2 - 5-12hrs

Type 3 - 3-8hrs

Type 4 - 24-48hrs

24
Q

Give a brief describption of type 1 hypersensitivity

A

Typically known as ‘Allergic reaction’

Environmental, non-infectious antigens trigger mast cell response

IgE mediated

25
Q

Give a brief description of type 2 hypersensitivity

A

IgG or IgM mediated

IgG or IgM bind to antigen on a target cell which is in fact a host cell

Cell mediated immune response occurs

26
Q

Give a brief description of type 3 hypersensitivity

A

Reaction to the formation of Immune complexes (Soluble antigen and antibody)

When not adequately cleared from circulation by macrophages can be deposited in tissues giving rise to an inflammatory reaction

27
Q

Give a brief description of type 4 hypersensitivity

A

Cell mediated immune response to environmental antigens and self antigens

In the case of self antigens, this can lead to the distruction of tissues via cytotoxic action of T cells

‘Autoimmune disease’

28
Q

Why do people have allergies?

A

Hygiene hypothesis:

In areas a good sanitation, High antibiotic use and as a result a population with a low helminth and faeco-oral burden Allergic disorders are more likely to occur as a result of the immune system not developing as it should

Conversely, in area of low sanitation, low antibiotic use etc there is a lower prevalence of allergy

Genetics:

Genetic factors seem to contribute to the production of TH1 phenotype (allergy resistant) and TH2 phenotpye (allergy prone)

TH2 phenotype is characterised by increased IgE levels, the mediator of Type 1 hypersensitivity reaction

29
Q

List some common allergens

A

House mites, dust, Animals (pets in particular)

Tree and grass pollen

Insect venom (stings)

Medicines (Penicillin)

Chemicals such as Latex

Foods (Milk, Peanuts, nuts)

30
Q

What is Allergic cross-reactivity?

Give an example

A

Often people with one allergy have an increased chance of having a related allergy

If someone is allergic to cow’s milk, there is 92% risk of reaction to goat’s milk

31
Q

What are some of the mast cell mediators involved in type 1 hypersensitivity reactions?

A

Enzymes (tryptase)

Histamine, Heparin

Cytokines (IL-1, TNF-a)

Leukotrienes

32
Q

Describe the 2 immune system mechanisms of allergic reactions

A

Indirect:

Allergen has 1st exposure and antibodies are created

Plasma cells persist production of specific IgE after antigen cleared

IgE binds to cell surface receptors of Mast cells ‘sensitising’ them

Second exposure causes crosslinking of mast cell bound IgE

Mast cell degranulation occurs triggering release of granules content (Histamine/Chemokines) and the synthesis of new mediators (Prostaglandins/Leukotrienes)

This leads to local or systemic effects such as increased vascular permeability, vasodilation and bronchial constriction

Direct:

As above however mast cell doesn’t need to be desensitised, Degranulation occurs in respinse to ‘irritants’ (E.g. C3a, C5a)

33
Q

Outline the skin prick test for allergy

A

Allergen is introduced in small amounts into patients skin via a pinprick on the skin

A wheal and flare reaction indicative of local allergic reaction is looked for

Size of reaction indicates severity of allergy

Needs trained personnel due to risk of anaphylaxis

34
Q

Give 2 skin manifestations of allergic reaction

A

Urticaria:

Raised, itchy wheals appear on the skin as a result of allergic reaction in the upper dermis

Angioedema:

rapid swelling (oedema) of the dermis, subcutaneous tissue, mucosa and submucosal tissues of the skin

Can lead to airway obstruction

35
Q

What are the effects of systemic activation of mast cells?

A

Anaphylaxis:

Hypotension (Cardiovascular collapse)

Generalised urticaria

Angioedema

Bronchial constriction (Wheezing and suffocation may result)

36
Q

What is the first line treatment for anaphylaxis?

List it’s actions

A

IM Adrenaline (Epipen):

Reverses peripheral vasodilation and reduces oedema

Reverses airway constriction/bronchospasm

Increases contractile force of myocardium

Inhibits mast cell activation

37
Q

Give 2 examples of respiratory allergic reactions and their common allergens

A

Allergic rhinitus:

Pollen

Dust mite faeces

Asthma:

Danders (cat)

Pollen

Dust mite faeces

38
Q

How is diagnoses of an allergy made?

A

Clinical history:

Atopy, allergens, seasonality, route of exposure

Blood tests:

Serum IgE

Serum Mast cell tryptase, histamine

Skin prick test:

Wheal and flare over >3mm

Challenge tests:

Give them the thing they’re allergic to and just see what happens

39
Q

Give some techniques for allergy management

A

Avoidance:

Read food packaging

Avoid high risk situations

Education:

EPIpen use (and calling the ambulance after!)

Parents to recognise symptoms

Medic alert ID

Densensitisation:

Repeat exposure to allergen to desensitise (highly controlled, highly effective)

Drugs:

Anti-histamines

Corticosteroids

Anti-IgE, IgG

Epipen

40
Q

Define Desensitisation

A

Administration of increasing dose of allergen extracts over a period of years given IV, Oral or Sublingual

90% effective in patients with Insect venom Anaphylaxis

ESA 3 (54 decks)

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